Size | Price | Stock | Qty |
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1mg |
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5mg |
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10mg |
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50mg |
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Other Sizes |
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ln Vitro |
Without altering the baseline glutamate release, preincubating synaptosomes with AMN082 (1 μM) for 10 min prior to 4-aminopyridine treatment efficiently suppresses 4-aminopyridine-evoked glutamate release [2].
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ln Vivo |
AMN082 (6 mg/kg; oral) generates a rise in stress hormones in a mGluR7+/+ mouse (C57BL/6 genetic background) in a mGluR7-dependent way [1]. AMN082 (1.25-5.0 mg/kg, i.p.; 30 minutes before each injection of cocaine or morphine during repeated dosing or before cocaine or morphine challenge) dose-dependently attenuates the development and expression of cocaine or morphine locomotor sensitization [3] .
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Animal Protocol |
Animal/Disease Models: Male Swiss mice (20-25g) [3]
Doses: 1.25, 2.5, 5.0 mg/kg Route of Administration: intraperitoneal (ip) injection; on day 17 or day 20, cocaine (10 mg/kg) or Results of morphine (10 mg/kg) given 30 minutes before challenge: Dramatically attenuated the expression of cocaine-induced locomotor sensitization; attenuated morphine-induced sensitization. |
References |
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Additional Infomation |
AMN082 dihydrochloride is a hydrochloride obtained by combining N,N'-bis(diphenylmethyl)ethane-1,2-diamine with two molar equivalent of hydrochloric acid. It has a role as a metabotropic glutamate receptor agonist, a geroprotector and a neuroprotective agent. It contains a N,N'-bis(diphenylmethyl)ethane-1,2-diamine(2+).
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Molecular Formula |
C28H28N2.2[HCL]
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Molecular Weight |
465.4572
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Exact Mass |
464.179
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CAS # |
97075-46-2
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Related CAS # |
AMN082 free base;83027-13-8
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PubChem CID |
11698390
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Appearance |
White to off-white solid powder
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LogP |
8.13
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Hydrogen Bond Donor Count |
4
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Hydrogen Bond Acceptor Count |
2
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Rotatable Bond Count |
9
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Heavy Atom Count |
32
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Complexity |
362
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Defined Atom Stereocenter Count |
0
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InChi Key |
YRQCDCNQANSUPB-UHFFFAOYSA-N
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InChi Code |
InChI=1S/C28H28N2.2ClH/c1-5-13-23(14-6-1)27(24-15-7-2-8-16-24)29-21-22-30-28(25-17-9-3-10-18-25)26-19-11-4-12-20-26;;/h1-20,27-30H,21-22H2;2*1H
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Chemical Name |
N,N'-dibenzhydrylethane-1,2-diamine;dihydrochloride
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HS Tariff Code |
2934.99.9001
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Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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Solubility (In Vitro) |
DMSO : ~33.33 mg/mL (~71.61 mM)
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Solubility (In Vivo) |
Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.
Injection Formulations
Injection Formulation 1: DMSO : Tween 80: Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)(e.g. IP/IV/IM/SC) *Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution. Injection Formulation 2: DMSO : PEG300 :Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline) Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil) Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals). View More
Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)] Oral Formulations
Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium) Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals). View More
Oral Formulation 3: Dissolved in PEG400  (Please use freshly prepared in vivo formulations for optimal results.) |
Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
1 mM | 2.1484 mL | 10.7421 mL | 21.4841 mL | |
5 mM | 0.4297 mL | 2.1484 mL | 4.2968 mL | |
10 mM | 0.2148 mL | 1.0742 mL | 2.1484 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration: mg/mL;
Method for preparing DMSO stock solution: mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation::Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O,mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
AMN082 activates G protein signaling via mGluR7. (A) Effect of DL-AP4 (4 mM, dotted line) and AMN082 (0.01-3 μM, solid line) on the inhibition of forskolin-stimulated cAMP accumulation in CHO cells stably expressing mGluR7b. (B) Effect of l-glutamate (L-Glu) and AMN082 on CHO mGluR2 cells. The results are normalized to control (30 μM forskolin-stimulated cAMP levels) and were pooled from at least six measurements obtained in three independent experiments and expressed as means with SEM. **, P < 0.01 vs. control; Dunnett's t test. (C) GTPγ35S binding experiments using membranes from CHO mGluR7b cells. The indicated concentrations of AMN082, DL-AP4, and l-glutamate were applied alone and in combination with each other. Three independent experiments were combined, and means with SEM are shown. Statistics symbols are shown for coapplication of drugs as follows: **, P < 0.01 vs. 8 mM l-glutamate (control); ##, P < 0.01 vs. 5 mM DL-AP4 (Dunnett's t test). (D) Concentration-response curves of AMN082 in the presence of 0.2 mM DL-AP4 with and without CPPG or MSOP, when using GTPγ35S binding on CHO mGluR7b membranes; mean data ± SEM from a single representative experiment (n = 3). (E and F) Chemical structures of L-AP4 and AMN082.[1].A selective metabotropic glutamate receptor 7 agonist: activation of receptor signaling via an allosteric site modulates stress parameters in vivo. Proc Natl Acad Sci U S A. 2005;102(51):18712-18717. td> |
AMN082 and orthosteric l-glutamate (L-Glu) site ligands have little, if any, effect on each other's potency. All membranes were prepared from CHO cells stably expressing mGluR7b. (A) Concentration-response curves for AMN082, DL-AP4, and l-glutamate. At least three independent experiments were pooled, and all values were normalized to the control stimulation of 8 mM l-glutamate (set to 100%); means with SEM are shown. (B) Concentration-response curves for AMN082 in the absence and presence of 3 mM l-glutamate concentrations. Three independent experiments were pooled, and all values were normalized as above; means with SEM are shown. (C) Concentration-response curves for l-glutamate in the absence and presence of 1 μM AMN082. Four independent experiments were pooled, and all values were normalized to control (as above). (B and C) □, no further chemicals were added. (D) The calculated parameters from at least three separate experiments, parts of which are shown in B and C, indicate that l-glutamate or AMN082 had little effect on AMN082 or l-glutamate potency, respectively. 95% CI, 95% confidence interval.[1].A selective metabotropic glutamate receptor 7 agonist: activation of receptor signaling via an allosteric site modulates stress parameters in vivo. Proc Natl Acad Sci U S A. 2005;102(51):18712-18717. td> |
AMN082 activates G protein signaling via a binding site in the transmembrane region of mGluR7. (A and B) The effect of AMN082 on GTPγ35S binding in the absence and presence of DL-AP4 when using membranes from CHO-C4 cells stably expressing mGluR7b (A) or mGluR6 (B). (C and D) The effect of AMN082 on mGluR6/7b (C) and mGluR7/6 (D) chimeric receptor cell membranes. All bars represent the mean ± SEM of at least three independent experiments (n = 3), and all values were normalized to the control stimulation of the respective agonist concentrations (4 mM DL-AP4 for mGluR7 and mGluR7/6; 10 μM DL-AP4 for mGluR6 and mGluR6/7b). **, Significant increases vs. maximal DL-AP4 controls (P < 0.01); ##, P < 0.01 vs. additive effect of submaximal DL-AP4 (gray bars) and 3 μM AMN082 (black bars); Dunnett's t test.[1].A selective metabotropic glutamate receptor 7 agonist: activation of receptor signaling via an allosteric site modulates stress parameters in vivo. Proc Natl Acad Sci U S A. 2005;102(51):18712-18717. td> |